Medico

The

n ew england journal

of

m edicine

r eview article

c urrent concepts

Management of Cirrhosis and Ascites
Pere Ginès, M.D., Andrés Cárdenas, M.D., Vicente Arroyo, M.D.,
and Juan Rodés, M.D.
From the Liver Unit, Hospital Clinic and
University of Barcelona, Institut d’Investigacions Biomèdiques August Pi-Sunyer,
Barcelona, Spain (P.G., A.C., V.A., J.R.); and
the Divisionof Gastroenterology and Hepatology, Beth Israel Deaconess Medical
Center and Harvard Medical School, Boston (A.C.). Address reprint requests to Dr.
Ginès at the Liver Unit, Hospital Clinic,
Villarroel 170, 08036 Barcelona, Spain, or
at gines@medicina.ub.es.
N Engl J Med 2004;350:1646-54.
Copyright © 2004 Massachusetts Medical Society.

c

irrhosis, most frequently caused by hepatitis c oralcoholism,
was the 12th leading cause of death in the United States in 2000, accounting
for more than 25,000 deaths.1 Ascites is the most common complication of
cirrhosis and is associated with a poor quality of life, increased risks of infections and
renal failure, and a poor long-term outcome.2,3 In recent years, important advances
have been made in the management of cirrhosis andascites.

pathophy siology of ascites
The chief factor contributing to ascites is splanchnic vasodilatation.4 Increased hepatic
resistance to portal flow due to cirrhosis causes the gradual development of portal hypertension, collateral-vein formation, and shunting of blood to the systemic circulation.
As portal hypertension develops, local production of vasodilators, mainly nitric oxide,increases, leading to splanchnic arterial vasodilatation.5 In the early stages of cirrhosis,
splanchnic arterial vasodilatation is moderate and has only a small effect on the effective arterial blood volume, which is maintained within normal limits through increases
in plasma volume and cardiac output.4 In the advanced stages of cirrhosis, splanchnic arterial vasodilatation is so pronounced that theeffective arterial blood volume decreases
markedly, and arterial pressure falls. As a consequence, arterial pressure is maintained
by homeostatic activation of vasoconstrictor and antinatriuretic factors, resulting in sodium and fluid retention. The combination of portal hypertension and splanchnic arterial vasodilatation alters intestinal capillary pressure and permeability, facilitating theaccumulation of retained fluid within the abdominal cavity. As the disease progresses,
there is marked impairment in renal excretion of free water and renal vasoconstriction —
changes that lead to dilutional hyponatremia and the hepatorenal syndrome, respectively4,6 (Fig. 1).

evaluation of patients with ascites
g eneral assessment

The evaluation of patients with cirrhosis and ascites shouldinclude not only an assessment of liver function but also an assessment of renal and circulatory function (Table 1).
Ideally, patients should be evaluated when they are not receiving diuretic agents, since
some variables related to renal function may be altered by the administration of these
medications. Ascitic fluid should be examined to rule out spontaneous bacterial peritonitis in patientswith new-onset ascites, whether or not they are hospitalized, and especially in those who have signs of infection, abdominal pain, encephalopathy, or gastrointestinal bleeding.

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Downloaded from www.nejm.org by JORGE MEJIA VELASQUEZ MD on March 22, 2007 .
Copyright © 2004 Massachusetts Medical Society. All rights reserved.

current concepts

Cirrhosis

Increased resistance
to portal flow

Portal hypertension

Splanchnic vasodilatation

Increase in splanchnic
capillary pressure

Arterial underfilling

Lymph formation that
exceeds lymph return

Arterial and cardiopulmonary receptors

Activation of vasoconstrictor
and antinatriuretic factors

Ascites

Sodium and water retention

Impaired...